Spatial learning ability of rats following acute exposure to alcohol during early postnatal life

Pauli, J. V.; Wilce, Peter A.; Bedi, K. S.

doi:10.1016/0031-9384(95)00120-8

Cited by 40 publications

(36 citation statements)

References 44 publications

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“…These findings correspond with previous research demonstrating impaired spatial learning and memory in E animals on the Morris water maze (Blanchard et al, 1990;Gianoulakis, 1990;Kim et al, 1997;Blanchard et al, 1987). Deficits in spatial ability also have been shown following neonatal ethanol exposure (Goodlett & Johnson, 1997;Goodlett & Peterson, 1995;Pauli, Wilce, & Bedi, 1995;Tomlinson, Wilce, & Bedi, 1998). Although deficits following prenatal ethanol exposure may not always appear in relatively simple spatial FIGURE 2 Annulus crossings on Day 4 (mean AE SEM) for E, PF, and C males in H and NH treatments at 2 (Young; top panels) or 13 to 14 (Mid-Aged; bottom panels) months of age (ns ¼ 8-10 in each Prenatal Group Â Postnatal Treatment).…”

Section: Discussionsupporting

confidence: 92%

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

Gabriel

Johnston

Weinberg

2002

Developmental Psychobiology

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Prenatal ethanol exposure results in spatial navigation deficits in young and mid-aged animals. In contrast, postnatal handling attenuates spatial deficits that emerge with age in animals that are not handled. Therefore, we investigated the ability of handling to attenuate spatial deficits in animals prenatally exposed to ethanol (E). Sprague-Dawley male offspring from E, pair-fed (PF), and control (C) groups were handled (H) or nonhandled (NH) from 1 to 15 days of age and tested on the Morris water maze at 2 or 13 to 14 months of age. In young animals, H-E males had longer latencies to locate the submerged platform, and E animals, across handling conditions, showed altered search patterns compared to their PF and C counterparts. Mid-aged animals had longer latencies than young animals, with no differences among E, PF, and C animals. However, corticosterone levels were higher in mid-aged E than in C males. Handling did not attenuate impairments associated with either prenatal ethanol exposure or aging.

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Section: Discussionsupporting

confidence: 92%

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

Gabriel

Johnston

Weinberg

2002

Developmental Psychobiology

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“…The precise functional consequences (if any) of their loss and subsequent replacement by new cells remain unknown. However, we previously reported (Pauli et al, 1995b;Tomlinson et al, 1998) that exposure of rats to ethanol can have deleterious effects on spatial learning behaviour, as measured in the Morris water maze (Morris, 1981;Morris et al, 1982). Stressful situations have also been shown to impair spatial learning ability (Luine et al, 1994;Diamond et al, 1996).…”

Section: _________________________________________________ Ethanol Exmentioning

confidence: 95%

“…As a consequence, we have been engaged for a number of years in examining both the short-term and long-term effects of exposure to ethanol on the rat brain at various periods of time during the first 2 weeks of postnatal life. For example, we previously reported (Pauli et al, 1995b;Tomlinson et al, 1998) that a high dose of ethanol exposure to rats during early postnatal life can result in long-lasting alterations in spatial learning ability as tested on the Morris water maze (Morris 1981;Morris et al, 1982). The question arises whether such behavioural deficits are accompanied by measurable morphological changes in the brains of these animals.…”

Section: Introductionmentioning

confidence: 95%

Effects of alcohol exposure during early life on neuron numbers in the rat hippocampus. I. Hilus neurons and granule cells

et al. 2003

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We previously showed that 16-day-old rats exposed to a relatively high dose of ethanol at 10-15 postnatal days of age have fewer neurons in the hilus region of the hippocampus compared with controls. Dentate gyrus granule cell numbers, however, showed no statistically significant changes attributable to the ethanol treatment. It is possible that some of the changes in brain morphology, brought about as a result of the exposure to ethanol during early life, may not be manifested until later in life. This question has been further addressed in an extension to our previous study. Wistar rats were exposed to a relatively high daily dose of ethanol on postnatal days 10-15 by placement in a chamber containing ethanol vapour, for 3 h/day. The blood ethanol concentration was found to be approximately 430 mg/dl at the end of the period of exposure. Groups of ethanol-treated (ET), separation control (SC), and mother-reared control (MRC) rats were anaesthetised and killed either at 16 or 30 days of age by perfusion with phosphate-buffered 2.5% glutaraldehyde. The Cavalieri principle and the physical disector methods were used to estimate, respectively, the regional volumes and neuron cell numerical densities in the hilus and granule cell regions of the dentate gyrus. The total numbers of neurons in the hilus region and granule cell layer were computed from these estimates. It was found that 16-day-old animals had 398,000-441,000 granule cells, irrespective of group. The numbers of granule cells increased such that by 30 days of age, rats had 487,000-525,500 granule cells. However, there were no significant differences between ethanol-treated rats and their age-matched controls in granule cell numbers. In contrast, ethanol-treated rats had slightly but significantly fewer neurons in the hilus region than did control animals at 16 days of age, but not at 30 days of age. Therefore, it appears that a short period of ethanol exposure during early life can have effects on neuron numbers of some hippocampal neurons, but not others. The effects on hilar neuron numbers, observed as a result of such short periods of ethanol treatment, appeared to be transitory.

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“…However, the duration of exposure was important, in that males exposed to alcohol over 2 postnatal days (i.e., PN4-6 or PN7-9) also showed spatial learning deficits, whereas the full exposure period (i.e., PN4-9) was required to reveal deficits in females. Even a single neonatal day of alcohol exposure on either PN5 or PN10 may be sufficient to impair Morris maze performance in male rats tested between 41-54 days of age (Pauli et al, 1995).…”

Section: Dose Gender Effects and Critical Periods Of Exposurementioning

confidence: 99%

Effects of prenatal alcohol exposure on the hippocampus: Spatial behavior, electrophysiology, and neuroanatomy

2000

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Prenatal exposure to alcohol can result in fetal alcohol syndrome (FAS), characterized by growth retardation, facial dysmorphologies, and a host of neurobehavioral impairments. Neurobehavioral effects in FAS, and in alcohol‐related neurodevelopmental disorder, include poor learning and memory, attentional deficits, and motor dysfunction. Many of these behavioral deficits can be modeled in rodents. This paper reviews the literature suggesting that many fetal alcohol effects result, at least in part, from teratogenic effects of alcohol on the hippocampus. Neurobehavioral studies show that animals exposed prenatally to alcohol are impaired in many of the same spatial learning and memory tasks sensitive to hippocampal damage, including T‐mazes, the Morris water maze, and the radial arm maze. Direct evidence for hippocampal involvement is provided by neuroanatomical studies of the hippocampus documenting reduced numbers of neurons, lower dendritic spine density on pyramidal neurons, and decreased morphological plasticity after environmental enrichment in rats exposed prenatally to alcohol. Electrophysiological studies also demonstrate changes in synaptic activity in in vitro hippocampal brain slices isolated from prenatal alcohol‐exposed animals. Considered together, these observations demonstrate that prenatal exposure to alcohol can result in abnormal hippocampal development and function. Such studies provide a better understanding of neurological deficits associated with FAS in humans, and may also contribute to the development of strategies to ameliorate the effects of prenatal alcohol exposure on behavior. Hippocampus 2000;10:94–110. © 2000 Wiley‐Liss, Inc.

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Spatial learning ability of rats following acute exposure to alcohol during early postnatal life

Cited by 40 publications

References 44 publications

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

Prenatal ethanol exposure and spatial navigation: Effects of postnatal handling and aging

Effects of alcohol exposure during early life on neuron numbers in the rat hippocampus. I. Hilus neurons and granule cells

Effects of prenatal alcohol exposure on the hippocampus: Spatial behavior, electrophysiology, and neuroanatomy

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